Expression of NCR2 and the immune checkpoint TIM3/LGALS9 in Chronic Myeloid Leukemia patients during the first year of treatment with Imatinib

TOLOZA, MARIA JAZMIN; BESTACH, YESICA; LINCANGO YUPANKI, MARCO; CAMACHO, MARÍA FERNANDA; BORDONE, JAVIER; MARIANO, ROMINA; TARQUI, M; PEREZ, MARIEL; ARANGUREN, PEDRO NEGRI; ENRICO, ALICIA; LARRIPA, IRENE; BELLI, CAROLINA B

Mar del Plata

Congreso; Reunión Conjunta SAIC, SAI, FAIC, SAFIS; 2022

SAIC

Our previous results evaluating T-cell responses showed a suppression in Chronic Myeloid Leukemia (CML) at diagnosis. A slow restoration of this compartment after imatinib initiation was observed with some mediators requiring more than one year to normalize. Interestingly, responders displayed some components differentially expressed (i.e. ARG1, TNF or IL6).The aim was to include TIM3/LGALS9, important member of the immune checkpoints in myeloid leukemia, and NCR2, a cytotoxicity-activating receptor that contribute to efficiency of activated natural killer cells.Total RNA from peripheral blood samples was collected from 89 CML patients (41 serially followed) at diagnosis (n:28) or under treatment at 3 (n:50), 6 (n:50) or 12 (n:44) months classified according to the molecular response at each time. Gene expression was evaluated by quantitative real-time PCR applying the comparative method 2-ΔCT relative to GAPDH gene. Statistical analyses were performed using the InfoStat software v2019 and p-values